Overexpression of long non‑coding RNA H19 enhances cell viability and inhibits apoptosis in recurrent spontaneous abortion by targeting the miR-29a-3p/SOCS3 axis.

Abstract

Recurrent spontaneous abortion (RSA) represents a substantial challenge in reproductive medicine, attributed to a variety of complex factors, among which aberrations in long non-coding RNAs (lncRNAs) play a crucial role. The present study delves into the functional dynamics of the lncRNA H19 in the context of RSA, particularly focusing on its regulatory interplay with miR-29a-3p and the Suppressor of Cytokine Signaling 3 (SOCS3). A notable downregulation of H19 in villous tissues from RSA patients was observed, highlighting its potential involvement in RSA pathophysiology. Functional assays demonstrated that overexpression of H19 in HTR-8/SVneo cells enhances cellular viability while concurrently attenuating apoptotic processes, thereby indicating a pivotal role of H19 in cellular survival pathways. This study identifies miR-29a-3p as a direct regulatory target of H19, exerting significant influence on cellular viability and apoptosis. The inhibition of miR-29a-3p was observed to mitigate its pro-apoptotic effects, thereby reinforcing its critical regulatory capacity in cellular homeostasis. Moreover, SOCS3 was delineated as a downstream effector of miR-29a-3p, with its expression being inversely modulated by miR-29a-3p. Co-transfection experiments involving H19, miR-29a-3p, and SOCS3 unraveled their intricate regulatory nexus in modulating cellular survival mechanisms. Collectively, these findings elucidate that H19 orchestrates the regulation of cell viability and apoptosis in RSA through the miR-29a-3p/SOCS3 signaling axis, thereby providing valuable insights into the molecular underpinnings of RSA and unveiling novel avenues for therapeutic intervention.